GROUP THREE

IKWARA EMMANUEL ASHER 19/U/0057/PHL

JOLLY JUDITH 18/U/0546/PHL/PS
NAKWANG IRENE FOURTUNATE 19/U/0322/PHL/PS
AYO NELSON 19/U/0080/PHL
MUHINDO MUARINE 19/U/0064/PHL.
 OCD
• Anxiety disorder
• Recurrent obsessions or compulsions that are severe enough to be time
consuming or to cause marked distress or significant impairment.
• Obsessions are unwanted, intrusive, persistent ideas, thoughts, impulses or
images that cause marked distress.
• Compulsions are unwanted repetitive behavior patterns or mental acts that are
intended to reduce anxiety, not to provide pleasure or gratification.
• Affects 3% globally.
• Starts any time from childhood.
• Normally associated with schizophrenia and depression.
 CLASSIFICATION ICD 9
• F42 OCD
• F42.0 Predominantly obsessive thoughts or ruminations
• F42.1 Predominantly compulsive acts.
• F42.2 Mixed obsessional thoughts and acts.
• F42.8 other obsessive compulsive disorder
• F42.9 obsessive compulsive disorder, unsatisfied.
 CAUSES OF OCD
The exact cause of OCD is not clear. Possible causes include the following;
• It can be genetical
• Irregular development and impairment of some parts of the brain
• Serotonin deficiency associated with anxiety disorders
• The body changes affecting the normal chemistry and biological
functioning of the body)
• Past childhood experiences
NB: Serotonin is a neural transmitter that helps to regulate mood and sleep
 ETIOLOGICAL FACTORS

• Psychoanalytical theory

• Learning theory

• Biological aspects i.e. neuroanatomy, physiology and biochemical factors

 PSYCHOANALYTICAL THEORY
OCD patients have,
• Weak, underdeveloped egos
• Reasons: unsatisfactory parent child relationship, conditional love
• Regression to the pre oedipal anal sadistic phase, combined with use of
specific ego defense mechanisms (displacement, reaction formation,
undoing, isolation), produces the clinical symptoms of obsessions and
compulsions.
 LEARNING THEORY

• It explains OCD patients as a conditioned response to traumatic event.

• Traumatic event produces anxiety and discomfort

• Passive avoidance i.e. staying away from the source

• Active avoidance i.e. staying with the source

 BIOLOGICAL ASPECTS

• Neuroanatomy: Neuroimaging techniques have

shown abnormal metabolic rates in the basal
ganglia and orbital frontal cortex of individuals
with the disorder.
 CONT.
• Physiology: Electrophysiology studies, sleep
electroencephalogram studies, and neuroendocrine studies have
suggested that there are commonalities between depressive
disorder and OCD. Neuroendocrine commonalities were
suggested in studies in which about one third of OCD clients
show non suppression test and decreased growth hormone
secretion with clonidine infusions.
 BIOLOGICAL ASPECT
• Biological factors: The neurotransmitter serotonin as influential in the etiology of OCD
behaviors.
 S/S OF OBSESSIONS
• Repeated thoughts about contamination
• Repeated doubts
• A need to have things in a certain order.
• Thought of aggression
• Sexual imagery
 S/S OF COMPULSIONS

• Washing and cleaning e.g. excessive hand washing or house cleaning

• Counting like counting the number of times that something is done.

• Checking like checking for what some one has done over and over again.

• Requesting or demanding assurance from others

• Repeating actions e.g. going in and out of door or up and down from a chair.
 CLINICAL FEATURES
• Obsessional thought
• Obsession ruminations
• Obsessional doubts
• Obsessional impulses
• Obsessional rituals
• Obsessional slowness
 DIAGNOSTIC CRITERIA
Specific criteria to be clinically diagnosed.
• Anxiety disorder with presence of obsessions or compulsions
• Ego dystonic i.e. realize thoughts and actions are irrational or excessive
• Must take up more than one hour a day.
• Must disrupt daily routine
• Symptoms cant result from effects of other medical conditions or
substances
 OBSSESSIVE COMPULSIVE
DISORDER MANAGEMENT.

• Behavioral therapy

• Cognitive therapy

• medication
 COGNITIVE BEHAVIORAL
THERAPY
• Cognitive: Change the way they think or deal with their fears

• Behavioral: Change the way they react to anxiety provoking situations

• Exposure and response prevention i.e. slowly learning to tolerate anxiety associated with not

performing ritual behavior e.g. Flooding and Systematic desensitization i.e. learning cognitive

strategies to deal with anxiety then gradual exposure to feared objects.

• Psychotherapy i.e. Talking with therapist to discover what causes the anxiety and how to deal with

symptoms.
 MEDICATION

• Anxiolytic benzodiazepine e.g. diazepam that give temporary relief

from anxiety though not effective on OCD

• Antidepressants to deal with depression like clomipramine

• Selective serotonin reuptake inhibitors.

 DELIRIUM
• Delirium is an acute organic mental disorder characterized by impairment of consciousness, disorientation and
disturbances in perception and restlessness.

• Hence delirium is a disturbance in consciousness and a change in cognition that develops over a short time.

Incidence

• Delirium has the highest incidence among mental disorders. About 10 to 25% of medical surgical inpatients, and
about 20 to 40% of geriatric patients meet the criteria for during hospitalization.

• Although delirium may occur in any age group, it is most common among the elderly.

Prevalance

• Estimated prevalence rates range from 10% to 30% of patients.

• 60%of those older than the age of 75 years.

 ETIOLOGY

Delirium is an abrupt onset of mental disorder due to any of several

general medical conditions e.g.
• HIV/AIDS
• Liver disease
• Renal failure
• Septicemia
• Meningitis
 CON’T
• Vascular: Hypertensive encephalopathy, intracranial hemorrhage
• Infections: Encephalitis, meningitis
• Neoplastic: Space occupying lesions
• Intoxication: Chronic intoxication or withdrawal effect of sedative hypnotic drugs.
• Traumatic: Subdural and epidural hematoma, contusion, laceration, postoperative, heat
stroke.
• Vitamin deficiency: For example thiamine.
• Endocrine and metabolic: diabetic coma and shock, uremia, myxedema, hyperthyroidism,
hepatic failure.
• Metals: heavy metals like lead, manganese and mercury.
• Carbon monoxide and toxins.
• Anoxia: Anemia, pulmonary or cardiac failure.
 FEATURES

• Disorientation in time, place and person.

• Poor concentration, apathy and over activity.
• Short attention span, absence mindedness, inability to learn new
information.
• Poor short term memory, inability to remember or recall information.
• Acute onset of illness.
 RISK FACTORS
Predisposing factors
• Advanced age
• Dementia
• Functional impairment in activities of daily living
• Medical comorbidity
• History of alcohol abuse
• Male gender
• Sensory impairment (blindness, deafness
 CON’T
• Acute myocardial events
• Acute pulmonary events
• Bed rest
• Fluid and electrolyte disturbance (including dehydration)
• Drug withdrawal (sedatives, alcohol)
• Infection (especially respiratory, urinary)
 DIAGNOSTIC CRITERIA
• History collection: any history of head injury, meningitis etc.
• Mental status examination
• Neurological examination
• Haematological investigation
• Blood “Rh” type ( blood grouping)
• Blood glucose
• ESR
• CBC
• Urine examination
 CON’T
• Test for memory i.e. immediate, recent and remote
• Radiological examination
• X ray skull
• CT scan of skull
• MRI of skull
• Electroencephalophalography
• Brain biopsy
 PATHOPHYSIOLOGY

A range of different pathological circumstances may give rise to delirium

(Maldonado 2013).

• Leaky blood-brain barrier. Recent evidence suggests the blood-brain

barrier becomes leaky or disrupted as the brain ages, allowing exposure
to drugs and toxins. Also as a result of distal inflammation.
 CON’T
• Medications (wide range, esp. psychoactive, anticholinergic and opioids)
• Uncontrolled pain
• Urinary retention, faucal impaction
• Indwelling devices (urinary catheters)
• Severe anemia
• Use of restraints
• Intracranial events (stroke, bleeding, infection
 CON’T

• Imbalance of neurotransmitter production. Tryptophan competes

with the amino acid phenylalanine Pridmore. Disturbance of the
tryptophan: phenylamine ratio may increase or decrease the level of
serotonin resulting in delirium. Disturbance of the tryptophan:
phenylamine ratio has been observed in post traumatic states and other
medical and surgical conditions.
 CON’T

• Inflammation: Trauma and infection leads to increased production of

proinflammatory cytokines, which may produce delirium. Peripherally
secreted cytokines can cause responses from microglia, causing
inflammation of the brain. Cytokines affect the synthesis and release of a
wide range of neurotransmitters and also have neurotoxic.
 CON’T
• Elevated cortisol: Acute stress has been hypothesized as a cause of delirium. This is
consistent with the notion that elevated cortisol seen in PTSD results in hippocampal
shrinkage. The role of cortisol in delirium is under investigation (Maclullich et al,
2008).

• Neuronal injury caused by a variety of metabolic or ischemic insults.

• Other neurotransmitter abnormalities associated with delirium include elevated

dopamine function (haloperidol is effective in controlling symptoms). Possibly, also
NA and GABA
 CON’T

• Cholinergic deficiency: This is one of the best documented

mechanisms. It is seen in overdose of anticholinergic drugs, such as
atropine. It may also be seen with the use of drugs not primarily
classified as anticholinergics, but with clear cholinergic action:
antihistamines, some opioids and antidepressants.
 TREATMENT

1. Identification of cause and its immediate correction for example

50mg of 50% dextrose IV for hypoglycemia

 oxygen hypoxia

100mg of B1 IV for thiamine deficiency

Iv fluids for fluid and electrolyte imbalance.

 CON’T

2. Symptomatic measures:

Benzodiazepines(10mg diazepam or 2mg lorazepam IV)

The atypical antipsychotics like risperidone, olanzapine, quetiapine and aripiprazole

3. Other medications such as valproate, donepezil, or ondansetron may be effective and safe in

selected cases.
 MANAGEMENT
1. MEDICAL MANAGEMENT
The delirium management includes supportive therapy and pharmacological
management.
(a) Fluid and nutrition
These should be given carefully, because the patients may be unwilling or physically
unable to maintain a balance intake.
The patient suspected of having alcohol toxicity or alcohol withdrawal, therapy should
include multivitamins, especially thiamine.
(b) Environmental modification:
 CON’T
 Reorientation techniques or memory cues such as calendar, clocks, and family photos may
be helpful.
 The environment should be stable , quiet and well lighted, and also support from a familiar
nurse and family should be encouraged.
 Physical restrains should be avoided
 These patients should never live alone.
(c) Medication
 Neuroleptics: Haloperidol 0.5mg, P.O, BD/TDS.
Risperidone 0.5 to 2 mg, PO, QID or BD
 CON’T

• Short acting sedative : Lorazepam 0.5 to 2 mg, PO/IM/IV.

• Vitamins: Thiamine hydrochloride 100mg IV, followed by 50 to 100 mg/d, IV/IM, and cynocobalamine 1000mcg
IM monthly or 500mcg/wk intranasally or 100mcg/d, PO.

2. NURSING MANAGEMENT

A. Nursing Diagnosis

Risk for trauma to impairment of cognitive and psychomotor function.

Nursing intervention:

Store frequently use items within easy access.

Keep the dim light on at night

 CON’T
Soft restraints may be required if client is very disoriented and hyperactive.
Frequently orient the client to place, time and situations
B. Disturbed through process related to cerebral degeneration as evidenced by
disorientation, confusion, and memory deficits.
Frequently orient to reality
Use clock and calendars with large number that are easy to read.
Monitor for medication side effects.
Keep simple explanation
Talk about real people and real events.
 CON’T

Nursing intervention

• Provide guidance and assistance for independent action

• Provide the structural schedule of activities that does not change from day to day.

• Involve the family members in the care of the patients.

 DELIRIUM TREMENS

Delirium tremens is a psychotic condition caused by the complication from alcohol

withdrawal. It involves tremors, hallucination, anxiety , and disorientation.

Delirium tremens typically occurs in people with a high intake of alcohol for more than a
month.

When it occurs, it often lies for three days into the withdrawal syndromes and last for two to
three days.
 SIGNS AND SYMPTOMS

• Nightmares

• Disorientation

• Hallucinations

• Fever

• Confusion

• High blood pressure

 CAUSES

• Long periods of drinking alcohol and stopping suddenly

• Head injury

• Infections

• Illness in the people with a history of having use of alcohol

 FEATURES
• Clouding of consciousness with disorientation

• Poor attention span with distractibility

• Visual, tactile also hallucination and illusion

• Disturbance with tachycardia, fever, sweating, hypertension

• Shouting and evidence fear

• Insomnia

• Will have disorientation related to time and place

• Death may occur due to cardiovascular collapse, infection, hypertension, or self inflicted injury.
 MANAGEMENT OF DELIRIUM
TREMENS
 Keep the patients in a quiet and safe environment

 Sedation is usually given with diazepam 10mg, or lorazepam 4mg, IV or followed by oral
administration

 Maintain fluid and electrolyte balance

 Reassure patient and family

 CONCLUSION
• Delirium is the acute organic disorder characterized by impairment of the consciousness, disorientation
and disturbance in the perception and restlessness.

• Delirium has the highest incidence among organic mental disorders.

• About 10 t0 25% of medical surgical inpatients, and about 20 to 40% of geriatric patients meet the
criteria for delirium during hospitalization. A delirium is characterized by a disturbance of
consciousness, impairment of attention, and also emotional disturbance such as depression, fear,
irritability.

• Delirium tremens is a psychotic condition caused by the complications from alcohol withdrawal . It
involves tremors, hallucination, anxiety, and disorientation.
 REFERENCES

• Cavallazzi R, Saad M, Marik P. Delirium in the ICU: an overview. Annals of Intensive Care

2012; 2:49. Cerejeira J, Mukaetova-Ladinska E. A clinical update on delirium: from early

recognition to effective management. Nursing Research and Practice 2011: doi:

10.1155/2011/875196. Cerveira C et al. Delirium in the elderly. Dement Neuropsychol 2017;

11: 207-275. Eikelenboom P, Hoogendijk W. Do delirium and Alzheimer’s dementia share

specific